The Narrator learns that Tyler plans to erase debt by destroying buildings containing credit card records. He tries to warn Marla but she does not believe him. He goes to the police and is threatened by officers who reveal they are members of Project Mayhem, and escapes to try to disarm the explosives in one building but is subdued by Tyler and held at gunpoint on the top floor. The Narrator realizes that it is actually himself who is holding the gun, and he fires the weapon into his own mouth, blowing a hole through his cheek. Tyler stands motionless, smoke coiling from his head, and then collapses and vanishes. Marla arrives to find the Narrator badly wounded but alive. He tells her that she met him "at a very strange time" in his life, and they hold hands and watch as the buildings around them explode.
Filming lasted 138 days from July to December 1998,[45] during which Fincher shot more than 1,500 rolls of film, three times the average for a Hollywood film.[32] The locations were in and around Los Angeles and on sets built at the studio in Century City.[45] Production designer Alex McDowell constructed more than 70 sets.[32] The exterior of Tyler Durden's house was built in Wilmington, California,[46] while the interior was built on a sound stage at the studio's location. The interior was given a decayed look to illustrate the deconstructed world of the characters.[45] Marla Singer's apartment was based on photographs of apartments in downtown LA.[18] Overall, production included 300 scenes, 200 locations, and complex special effects. Fincher compared Fight Club to his subsequent, less complex film Panic Room: "I felt like I was spending all my time watching trucks being loaded and unloaded so I could shoot three lines of dialogue. There was far too much transportation going on."[47]
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Other visual effects include an early scene in which the camera flashes past city streets to survey Project Mayhem's destructive equipment lying in underground parking lots; the sequence was a three-dimensional composition of nearly 100 photographs of Los Angeles and Century City by photographer Michael Douglas Middleton. The final scene of the demolition of the credit card office buildings was designed by Richard Baily of Image Savant; Baily worked on the scene for over fourteen months.[48]
Fincher supervised the composition of the DVD packaging and was one of the first directors to participate in a film's transition to home media. The film was released on DVD on June 6, 2000, in one and two-disc editions.[70] The movie disc included four commentary tracks,[71] while the bonus disc contained behind-the-scenes clips, deleted scenes, trailers, theater safety PSAs, the promotional music video "This is Your Life", Internet spots, still galleries, cast biographies, storyboards, and publicity materials.[72] Fincher worked on the DVD as a way to finish his vision for the film. Julie Markell, 20th Century Fox's senior vice president of creative development, said the DVD packaging complemented Fincher's vision: "The film is meant to make you question. The package, by extension, tries to reflect an experience that you must experience for yourself. The more you look at it, the more you'll get out of it." The studio developed the packaging for two months.[73] The two-disc special edition DVD was packaged to look covered in brown cardboard wrapper. The title "Fight Club" was labeled diagonally across the front, and packaging appeared tied with twine. Markell said, "We wanted the package to be simple on the outside, so that there would be a dichotomy between the simplicity of brown paper wrapping and the intensity and chaos of what's inside."[73] Deborah Mitchell, 20th Century Fox's vice president of marketing, described the design: "From a retail standpoint, [the DVD case] has incredible shelf-presence."[74] It was the first DVD release to feature the THX Optimode.[75]
processing.... Drugs & Diseases > Cardiology Heart Failure Updated: Jul 02, 2022 Author: Ioana Dumitru, MD; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE more...
Share Email Print Feedback Close Facebook Twitter LinkedIn WhatsApp webmd.ads2.defineAd(id: 'ads-pos-421-sfp',pos: 421); Sections Heart Failure Sections Heart Failure Overview Practice Essentials
Background Pathophysiology Etiology Epidemiology Prognosis Patient Education Show All Presentation History
Physical Examination Predominant Right-Sided Heart Failure Heart Failure in Children Heart Failure Criteria, Classification, and Staging ACC/AHA Staging Show All DDx Workup Approach Considerations
Routine Laboratory Tests Natriuretic Peptides Genetic Testing Assessment of Hypoxemia Electrocardiography Chest Radiography Echocardiography CT Scanning and MRI Nuclear Imaging Catheterization and Angiography Assessment of Functional Capacity Show All Treatment Approach Considerations
Nonpharmacologic Therapy Pharmacologic Therapy Acute Heart Failure Treatment Treatment of Heart Failure with Preserved LVEF Treatment of Right Ventricular Heart Failure Electrophysiologic Intervention Revascularization Procedures Valvular Surgery Ventricular Restoration Extracorporeal Membrane Oxygenation Ventricular Assist Devices Heart Transplantation Total Artificial Heart Show All Guidelines Guidelines Summary
Screening and Genetic Testing Diagnostic Procedures Nonpharmacologic Therapy Pharmacologic Therapy Electrophysiologic Intervention Revascularization Procedures Valvular Surgery Mechanical Circulatory Support Devices Heart Transplantation Management of Acute Decompensated Heart Failure (ADHF) Show All Medication Medication Summary
Beta-Blockers, Alpha Activity Beta-Blockers, Beta-1 Selective ACE Inhibitors ARBs Inotropic Agents Vasodilators Nitrates B-type Natriuretic Peptides I(f) Inhibitors Angiotensin Receptor-Neprilysin Inhibitors (ARNi) Diuretics, Loop Diuretics, Thiazide Diuretics, Other Diuretics, Potassium-Sparing Aldosterone Antagonists, Selective SGLT2 Inhibitors Soluble Guanylate Cyclase Stimulators Alpha/Beta Adrenergic Agonists Calcium Channel Blockers Anticoagulants, Cardiovascular Opioid Analgesics Show All Questions & Answers Media Gallery Tables References Overview Practice Essentials Heart failure develops when the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure. See the image below.
Heart failure is the pathophysiologic state in which the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure.
Heart failure (see the images below) may be caused by myocardial failure but may also occur in the presence of near-normal cardiac function under conditions of high demand. Heart failure always causes circulatory failure, but the converse is not necessarily the case, because various noncardiac conditions (eg, hypovolemic shock, septic shock) can produce circulatory failure in the presence of normal, modestly impaired, or even supranormal cardiac function. To maintain the pumping function of the heart, compensatory mechanisms increase blood volume, cardiac filling pressure, heart rate, and cardiac muscle mass. However, despite these mechanisms, there is a progressive decline in the ability of the heart to contract and relax, resulting in worsening heart failure.
Signs and symptoms of heart failure include tachycardia and manifestations of venous congestion (eg, edema) and low cardiac output (eg, fatigue). Breathlessness is a cardinal symptom of left ventricular (LV) failure that may manifest with progressively increasing severity.
Laboratory studies for heart failure should include a complete blood count (CBC), electrolyte levels, and hepatorenal function studies. Imaging studies such as chest radiography and two-dimensional echocardiography are recommended in the initial evaluation of patients with known or suspected heart failure. B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels can be useful in differentiating cardiac and noncardiac causes of dyspnea. (See Workup for more information.)
In acute heart failure, patient care consists of stabilizing the patient's clinical condition; establishing the diagnosis, etiology, and precipitating factors; and initiating therapies to provide rapid symptom relief and survival benefit. Surgical options for heart failure include revascularization procedures, electrophysiologic intervention, cardiac resynchronization therapy (CRT), implantable cardioverter-defibrillators (ICDs), valve replacement or repair, ventricular restoration, heart transplantation, and ventricular assist devices (VADs). (See Treatment for more information.)
The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs.
In acute heart failure, the finite adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. [17] 2ff7e9595c
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